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目的观察醒脑静、丁苯酞及二者联合分别对大鼠脑缺血再灌注损伤后神经细胞凋亡及Bcl-2和Bax表达的影响。方法 60只雄性wistar大鼠(250±20)g采用改良线栓法制作脑缺血再灌注损伤模型(Middle cerebral artery occlusion,MCAO),随机分为4组,即模型组、醒脑静组、丁苯酞组、醒脑静联合丁苯酞(联合用药)组,每组又分为6、24、72h三个亚组;通过原位末端转移酶标记技术(TUNEL)检测神经细胞凋亡情况,采用免疫组化法观察大鼠脑缺血再灌注各个时间点Bcl-2、Bax的表达水平。结果 (1)模型组手术对侧大脑半球偶见凋亡细胞,病灶区可见大量神经细胞凋亡。丁苯酞用药组、醒脑静用药组凋亡细胞数明显减少,醒脑静联合丁苯酞组凋亡细胞数最少(P<0.05);(2)丁苯酞组及联合用药组Bcl-2阳性表达水平较模型组均有提高,联合用药组Bcl-2阳性表达水平在各时间点均最高(P<0.05);丁苯酞组及联合用药组Bax阳性表达水平较模型组均有降低,联合用药组Bax阳性表达水平最低(P<0.05)。结论 (1)醒脑静、丁苯酞及二者联合均可能通过抑制脑缺血再灌注损伤后神经细胞凋亡来实现神经细胞保护作用,其中二者联合效果最佳;(2)丁苯酞可能通过增加脑缺血再灌注损伤大鼠Bcl-2表达,减少Bax表达的方式来减少神经细胞凋亡,从而减轻脑缺血再灌注损伤;(3)醒脑静本身不能对Bcl-2、Bax的表达水平产生影响,但其可能通过增强丁苯酞作用的方式影响Bcl-2、Bax的表达,从而减轻脑缺血再灌注损伤。
Objective To observe the effects of xingnaojing, butylphthalide and their combination on neuronal apoptosis and expression of Bcl-2 and Bax after cerebral ischemia-reperfusion injury in rats. Methods Sixty male Wistar rats (250 ± 20) g were randomly divided into 4 groups (model group, xingnaojing group, Butylphthalide group, Xingnaojing combined with Butylphthalide (combination group), each group was divided into three subgroups: 6,24,72h. The apoptosis of nerve cells was detected by TUNEL Immunohistochemistry was used to observe the expression of Bcl-2 and Bax at various time points after cerebral ischemia / reperfusion in rats. Results (1) Apoptotic cells were occasionally seen in the contralateral hemisphere of the model group. A large number of apoptotic neurons were found in the lesion area. Butylphthalide treatment group, Xingnaojing group significantly decreased the number of apoptotic cells, Xingnao Jing combined with butylphthalide group the least apoptotic cells (P <0.05); (2) butylphthalide group and combination group Bcl- 2 expression in the combination group was significantly higher than that in the untreated group (P <0.05). The positive expression of Bcl-2 in the combination group was the highest at all time points , The lowest level of Bax was found in combination group (P <0.05). Conclusion (2) Xingnaojing, butylphthalide and the combination of the two may protect nerve cells by inhibiting apoptosis of neural cells after cerebral ischemia-reperfusion injury, and the combination of the two is the best; (2) Phthalide may reduce the apoptosis of nerve cells and relieve cerebral ischemia-reperfusion injury by increasing the expression of Bcl-2 and decreasing the expression of Bax in rats with cerebral ischemia-reperfusion injury. (3) Xingnaojing itself can not inhibit Bcl-2 , Bax, but it may affect the expression of Bcl-2 and Bax by enhancing the effect of butylphthalide, so as to relieve cerebral ischemia-reperfusion injury.